HSV encephalitis-induced anti-NMDAR encephalitis in a 67-year-old woman: report of a case and review of the literature

Abstract

Herpes simplex virus (HSV) encephalitis can induce an autoimmune encephalitis mediated by autoantibodies against the N-methyl-D-aspartate receptor (NMDAR). Post-HSV NMDAR encephalitis and de novo NMDAR encephalitis have been more commonly described in children and young adults. We describe the case of a 67-year-old woman with post-HSV NMDAR encephalitis and review the relevant literature. Clinical, serological, neurophysiological, and imaging evaluations were undertaken in the evaluation of this patient. A literature review was performed. Nearly 2 months after a typical course of HSV encephalitis confirmed by HSV polymerase chain reaction studies from the spinal fluid and treated with intravenous acyclovir, a 67-year-old woman suffered neurological deterioration. There was no evidence of active HSV infection, but NMDAR antibodies were found in her serum and spinal fluid. The patient improved after initiation of immunosuppressive therapy. All patients who experience new or recurrent neurological symptoms following recovery from HSV encephalitis should be evaluated for post-infectious autoimmune encephalitis, including NMDAR encephalitis.

Herpes simplex virus‐induced anti‐N‐methyl‐d‐aspartate receptor encephalitis: a systematic literature review with analysis of 43 cases

“…Our literature search led to the identification of 20 articles, published between 2013 and 2016, reporting a total of 42 patients who experienced biphasic disease with HSE followed by HSV‐induced anti‐NMDAR encephalitis . The full text of all articles was available.…”

“…[52][53][54][55] The possibility of a common genetic predisposition between the two entities may also contribute. 29 Different to the biphasic disease described above (HSE followed by HSV-induced anti-NMDAR encephalitis; Table SII, top part), in patients with HSE with concomitant detection of anti-NMDAR antibodies (in the absence of a clinical episode of anti-NMDAR encephalitis) the pathogenic role of antibodies remains unclear. 9,34 In particular, whether some of the clinical manifestations observed in these cases during HSE may be due to an additional effect of anti-NMDAR antibodies is not Review 801 known.…”

“…Our literature search led to the identification of 20 articles, published between 2013 and 2016, reporting a total of 42 patients who experienced biphasic disease with HSE followed by HSV-induced anti-NMDAR encephalitis. [14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33] The full text of all articles was available. With the addition of our case, a total of 43 patients with biphasic disease with HSE followed by HSV-induced anti-NMDAR encephalitis were identified (31 children).…”

Acute Flaccid Myelitis in the United States, August–December 2014: Results of Nationwide Surveillance

“…The detection of EV-D68 in CSF could have been hampered by delayed timing of specimen collection in relation to direct viral neuronal invasion and/or the relatively small number of samples to detect a transient presence of virus in CSF. Alternatively, neuronal damage could have been due to a postinfectious immune response; inflammatory damage to gray matter, although less common than to white matter, has increasingly been described in other syndromes [47–49]. …”

A Case of Anti-N-Methyl-D-Aspartate Receptor Encephalitis Triggered by Herpes Simplex Virus Encephalitis

“…There have been reported cases of anti-NMDA receptor encephalitis and HSE was considered a precursor to it since the first report in 2012 [1][2][3]. Now the more acceptable mechanism is a viral infection of the central nervous system, especially the herpes simplex virus (HSV) infection, leads to severe inflammation of the peripheral lobe and tissue necrosis which causes NMDA receptor antigenic determinant exposure and activate autoimmune response.…”